Phase II - PTH acts on bone and kidney to increase plasma levels of calcium. Increased levels of calcium act directly on parathyroid cells to inhibit secretion of PTH. Thus, there is a negative feedback control between plasma levels of calcium and PTH. The secretion of PTH is now known to be regulated by a cell-surface calcium receptor that enables parathyroid cells to detect and respond to changes in plasma calcium concentration. Compounds that target the parathyroid calcium receptor have potential utility in the treatment of both primary and secondary hyperparathyroidism (HPT). Secondary HPT is a disorder characterized by hyperplasia of the parathyroid glands and elevated levels of circulating PTH. The disease is most commonly seen as a consequence of chronic renal failure (CRF). The primary clinical consequence of secondary HPT is the development of of osteitis fibrosa cystica, which accounts for the majority of cases of renal osteodystrophy. In the setting of hyperphosphatemia, patients are at risk for soft-tissue calcification with complications involving the skin, tendons, muscles, vasculature, lungs, and heart.